This work investigates the effect of a soy-based probiotic drink (Enterococcus faecium CRL 183 and Bifidobacterium longum ATCC 15707) on the fecal microbiota composition, body weight and inflammatory parameters in diet-induced obese mice. The probiotic group had a lower body weight until 9th week of the study, reduced area and diameter of adipocytes, and showed a significant increase of IL-6 and IL-10 compared to the obesite non-treated group. The intake of a high-fat diet results in an increase of Lactobacillus spp. while the probiotic drink positively modulates the intestinal microbiota by maintaining the population of microorganisms belonging to the phylum Bacteroidetes and increases Bifidobacterium spp. Our study finds that the regular intake of this probiotic drink is able to reduce body weight gain and the size of adipocytes while modulating the fecal microbiota and the immune profile of animals, therefore acting in a beneficial manner in the control of obesity.

Cardiovascular disease is the leading cause of mortality in western countries. Metabolic syndrome (MS), characterized by hyperlipidemia, hypertension, obesity and hyperglycemia, is a significant risk factor for cardiovascular disease. Visceral adipose tissue play a key role in the development of metabolic syndrome since this tissue secrets a variety of bioactive substances named adipokines or adipocytokines such as leptin, resistin, adiponectin, tumor necrosis factor alfa (TNFa), and visfatin. Visfatin has been described recently and its role in cardiovascular disease is controversial and has not yet been fully elucidated. Studies in human and animal experimental models suggest that visfatin would have a key role in the pathologies associates with cardiovascular disease. This review is focused in the role of visfatin as well as the main dipocytokines with cardiovascular disease and metabolic syndrome.

Scope This study evaluated the capacity of dietary catechin (C), quercetin (Q), and the combination of both (CQ), to attenuate adipose inflammation triggered by high fructose (HFr) consumption in rats and by tumor necrosis factor alpha (TNF‐α) in 3T3‐L1 adipocytes. Methods and results In rats, HFr consumption for 6 wk caused dyslipidemia, insulin resistance, reduced plasma adiponectin, adiposity, and adipose tissue inflammation. Dietary supplementation with 20 mg/kg/day of C, Q, and CQ improved all these parameters. In 3T3‐L1 adipocytes, C and Q attenuated TNF‐α‐induced elevated protein carbonyls, increased proinflammatory cytokine expression (MCP‐1, resistin), and decreased adiponectin. The protective effects of C and Q on adipose inflammation are in part associated with their capacity to (i) decrease the activation of the mitogen‐activated kinases (MAPKs) JNK and p38; and (ii) prevent the downregulation of PPAR‐γ. In summary, C and Q, and to a larger extent the combination of both, attenuated adipose proinflammatory signaling cascades and regulated the balance of molecules that improve (adiponectin) or impair (TNF‐α, MCP‐1, resistin) insulin sensitivity. Conclusion Together, these findings suggest that dietary Q and C may have potential benefits in mitigating MetS‐associated adipose inflammation, oxidative stress, and insulin resistance.

Chronic obesity and Chagas disease (caused by the protozoan Trypanosoma cruzi) represent serious public health concerns. The interrelation between parasite infection, adipose tissue, immune system and metabolism in an obesogenic context, has not been entirely explored. A novel diet-induced obesity model (DIO) was developed in C57BL/6 wild type mice to examine the effect of chronic infection (DIO+I) on metabolic parameters and on obesity-related disorders. Dyslipidemia, hyperleptinemia, and cardiac/hepatic steatosis were strongly developed in DIO mice. Strikingly, although these metabolic alterations were collectively improved by infection, plasmatic apoB100 levels remain significantly increased in DIO+I, suggesting the presence of pro-atherogenic small and dense LDL particles. Moreover, acute insulin resistance followed by chronic hyperglycemia with hypoinsulinemia was found, evidencing an infection-related-diabetes progression. These lipid and glucose metabolic changes seemed to be highly dependent on TLR4 expression since TLR4-/- mice were protected from obesity and its complications. Notably, chronic infection promoted a strong increase in MCP-1 producing macrophages with a M2 (F4/80+CD11c-CD206+) phenotype associated to oxidative stress in visceral adipose tissue of DIO+I mice. Importantly, infection reduced lipid content but intensified inflammatory infiltrates in target tissues. Thus, parasite persistence in an obesogenic environment and the resulting host immunometabolic dysregulation may contribute to diabetes/atherosclerosis progression.

Matrix metalloproteinases (MMPs) play an important role during physiological tissue remodeling in embryonic development and angiogenesis, as well as in pathophysiological conditions such as obesity and development and vulnerability of atherosclerotic plaque. Moreover, MMP circulating levels have emerged as potential biomarkers of cardiovascular disease. MMP expression and activity are regulated by different factors such as insulin resistance and obesity. Expanded fat tissue has been demonstrated to be an active organ, where MMPs also exert a role in adipogenesis, angiogenesis, and proliferation of extracellular matrix (ECM). However, the lack of association between adipose tissue and plasma levels of some MMPs, specifically MMP-2 and MMP-9, suggests that this tissue is not a major contributor to circulating gelatinases. MMPs are also co-expressed or co-repressed in response to inflammatory adipocytokines, like adiponectin and leptin. Adiponectin may also play a protective role in plaque rupture through selectively increasing the tissue inhibitor of metalloproteinase (TIMP) expression. Leptin induces the expression of MMP-2 activators as well as the expression of MMP-2, MMP-9, and TIMP-1 in different human cells. Furthermore, sex hormones also participate in MMP regulation. In postmenopausal women, hormone replacement therapy produces an increase in MMP activity, leading to a breakdown in ECM homeostasis and accelerated progression of vascular pathologies. Besides, in men, an inverse relationship between testosterone levels and MMP-2 activity has been described. It is still necessary to go forward in the study of MMPs in different metabolic situations to corroborate their role as vulnerable plaque biomarkers.

Lipolysis is a catabolic reaction that is mediated by adipose triglyceride lipase (ATGL) and its inhibitor such as G0/G1 switch gene 2 (G0S2) protein during the first step of hydrolysis. The hydrophobic domain of G0S2 protein interacts and binds to the patatin-like domain in ATGL. Although conservation of the hydrophobic domain has been reported across species, sheep G0S2 amino acids and its hydrophobic domain have not been sequenced and studied. In this study, the hydrophobic region of G0S2 which plays an important role in inhibition of ATGL-mediated lipolysis was highly conserved as shown in other species. Phylogenetic analysis revealed that ruminant G0S2 proteins showed greater homologies within the ruminant species compared to other mammalian species. Moreover, adipose-specific expression of G0S2 for sheep was observed. Together with an abundant expression of ATGL protein in adipose tissue of sheep, G0S2 protein may play a critical role in inhibiting ATGL-mediated triacylglycerol (TAG) hydrolysis in the adipose tissue.

Modern lifestyle and diets have been associated with metabolic disorders and an imbalance in the normal gut microbiota. Probiotics are widely known for their health beneficial properties targeting the gut microbial ecosystem. The aim of our study was to evaluate the preventive effect of Lactobacillus kefiri (L. kefiri) administration in a fructose-rich diet (FRD) mice model. Mice were provided with tap water or fructose-added (20% w/v) drinking water supplemented or not with L. kefiri. Results showed that probiotic administration prevented weight gain and epidydimal adipose tissue (EAT) expansion, with partial reversion of the adipocyte hypertrophy developed by FRD. Moreover, the probiotic prevented the increase of plasma triglycerides and leptin, together with the liver triglyceride content. Leptin adipocyte secretion was also improved by L. kefiri, being able to respond to an insulin stimulus. Glucose intolerance was partially prevented by L. kefiri treatment (GTT) and local inflammation (TNFα; IL1β; IL6 and INFγ) was completely inhibited in EAT. L. kefiri supplementation generated an impact on gut microbiota composition, changing Bacteroidetes and Firmicutes profiles. Overall, our results indicate that the administration of probiotics prevents the deleterious effects of FRD intake and should therefore be promoted to improve metabolic disorders.

This work reports the effect of dietary Salba (chia) seed rich in n-3 -linolenic acid on the morphological and metabolic aspects involved in adipose tissue dysfunction and the mechanism/s underlying the impaired glucose and lipid metabolism in the skeletal muscle of rats fed a sucrose-rich diet (SRD). Rats were fed a SRD for 3 months. Thereafter, half the rats continued with SRD while in the other half, corn oil (CO) was replaced by chia seed for 3 months (SRD+chia). In control group, corn starch replaced sucrose. The replacement of CO by chia seed in the SRD reduced adipocyte hypertrophy, cell volume and size distribution, improved lipogenic enzyme activities, lipolysis and the antilipolytic action of insulin. In the skeletal muscle lipid storage, glucose phosphorylation and oxidation were normalized. Chia seed reversed the impaired insulin stimulated glycogen synthase activity, glycogen, glucose-6-phosphate and GLUT-4 protein levels as well as insulin resistance and dyslipidemia.

Purpose: Rats fed a long-term sucrose-rich diet (SRD) developed adipose tissue dysfunction. In the adipose tissue of these SRD-fed rats, the present study analyzed the possible beneficial effects of dietary Salba (chia) seeds in improving or reversing the depletion of antioxidant defenses, changes in pro-inflammatory cytokines and ROS production. Methods: Wistar rats were fed a SRD for 3 months. After that, half of the animals continued with the SRD until month 6, while in the other half, corn oil was replaced by chia seeds for 3 months (SRD + chia). A reference group consumed a control diet all the time. Results: Compared with the SRD-fed rats, the animals fed a SRD + chia showed a reduction in epididymal fat pad weight; the activities of antioxidant enzymes CAT, SOD and GPx returned to control values, while GR significantly improved; mRNA GPx increased, and both mRNA SOD and the redox state of glutathione returned to control values; a significant increase in the expression of Nrf2 was recorded. These results were accompanied by a decrease in XO activity and ROS contents as well as plasma IL-6 and TNF-α levels. Chia seeds reversed the decrease in PPARγ protein mass level and increased the n-3/n-6 fatty acids ratio of membrane phospholipids. Besides, dyslipidemia and insulin sensitivity were normalized. Conclusion: This study provides new information concerning some mechanisms related to the beneficial effects of dietary chia seeds in reversing adipose tissue oxidative stress and improving the adipose tissue dysfunction induced by a SRD.

The present study investigates the benefits of the dietary intake of soy protein on adipose tissue dysfunction in a rat model that mimics several aspects of the human metabolic syndrome. Wistar rats were fed a sucrose-rich diet (SRD) for 4 months. After that, half of the animals continued with SRD until month 8 while in the other half, casein protein was replaced by isolated soy protein for 4 months (SRD-S). A reference group consumed a control diet all the time. In adipose tissue we determined: i) the activities of antioxidant enzymes, gene expression of Mn-superoxide dismutase (SOD) and glutathione peroxidase (GPx), and glutathione redox state ii) the activity of xanthine oxidase (XO), ROS levels and the gene expression of NAD(P)H oxidase iii) the expression of the nuclear factor erythroid-2 related factor-2 (Nrf2). Besides, adiposity visceral index, insulin sensitivity, and tumor necrosis factor-α (TNF-α) in plasma were determined. Compared with the SRD-fed rats, the animals fed a SRD-S showed: activity normalization of SOD and glutathione reductase, improvement of mRNA SOD and normalization of mRNA GPx without changes in the expression of the Nrf2, and improvement of glutathione redox state. These results were accompanied by a normalization of XO activity and improvement of both the ROS production as well as TNF-α levels in plasma. Besides, adipocyte size distribution, adiposity visceral index and insulin sensitivity improved. The results suggest that soy protein can be a complementary nutrient for treating some signs of the metabolic syndrome.